Meningitis is very literally inflammation of the meninges. Something swollen in a closed space is never good, so it’s important to not miss meningitis when it presents.
Classic triad of meningitis
- Neck stiffness
- Mental status change – in babies this can be an increase in somnolence or irritability (unconsolably crying)
- E. coli*
- GBS (Group B strep)*
- Neisseria meningitidis
- Strep pneumoniae
- Staph aureus
- Gram neg bacilli
- Haemophilus influenza
- Viral (“aseptic”)
* These are the common ones in the neonatal period
- Positive Gram stain
- CSF white blood cell (WBC) count >1000/uL with a predominance of neutrophils
- Low CSF glucose concentration <40 mg/dL (2.2 mmol/L)
- Empiric treatment: high doses of a 3rd generation cephalosporin (cefotaxime, ceftriaxone) and vancomycin (this covers antibiotic-resistant S. pneumoniae, N. meningitidis, and Hib)
The danger zone on the face is a little triangle from the corners of the mouth up to the bridge of the nose. The reason it has such an epic name is because due to its venous drainage (from the facial veins and pterygoid plexus) there’s the possibility of infection traveling from that area into the cavernous sinus.
The cavernous sinuses (there’s one on each side) is an area posterior to the maxillary sinuses and lateral to the pituitary. It receives blood from the superior and inferior ophthalmic veins, superficial cortical veins and the basilar plexus. The blood then drains into the petrosal sinuses (you guessed it, there’s a superior and inferior one of those too) and then those drain into the internal jugular vein.
The thing about the cavernous sinuses a whole lot of important stuff passes through it.
- CN III (occulomotor)
- CN IV (trochlear)
- CN V1 (ophthalmic branch of trigeminal)
- CN V2 (maxillary branch of trigeminal)
- CN VI (abducens)
- Internal carotid (and the sympathetic fibres on the carotid)
This means that if you are so unfortunate as to have infection tract back into it, there can be some nasty consequences like meningitis and cavernous sinus thrombosis which will generally present as problems involving those nerves.
The abducens and carotid are more medial and thought to be more bathed in the warm loving venous drainage meaning these are generally the first to show signs of a problem a-brewin’.
The arm has too many muscles. It also has too many nerves.
The problem is that someone comes in with weakness or numbness and you need to think, “Where in the brain/spine/nerve root/bits of brachial plexus/terminal branch is the actual problem?!”
One of the ways to help suss this out is by testing the deep tendon reflexes.
- Only biceps reflex absent – might be problem with musculocutaneous nerve or C5
- Both brachioradialis and triceps absent – problem with the radial nerve
- Only triceps absent – potential problem with C7
Of course you should correlate the reflex findings with the sensory findings and motor strength (remember the good old ASIA exam for testing specific nerve roots) to help determine if it is a terminal branch issue or something higher up.
And don’t forget to grade those reflexes!
||Very brisk +/- Clonus
Generally upper motor neuron (UMN) lesions result in hyperreflexia while lower motor neuron (LMN) lesions result in hyporeflexia.
The Lateral Spinothalamic Pathway is an ascending spinal tract, carrying sensory information to the brain. It is typically depicted as a chain of three neurons: first-, second-, and third-order neurons.
This pathway mediates sensation of pain and temperature.
The first-order neurons in the pathway are located in the dorsal root ganglia at all spinal levels. Their axons ascend the tract of Lissauer, and synapse with second-order neurons.
The second-order neurons are located in the dorsal horn, and their axons immediately decussate via the ventral white commissure. These axons ascend the lateral funiculus and project to the ventral posterolateral (VPL) nucleus of the thalamus.
Some collaterals are sent to areas involved in arousal, namely the midbrain reticular formation, and the intralaminar nuclei of the thalamus (which then project to the caudatoputamen, and frontal and parietal cortex).
The third-order VPL neurons send axons through the posterior limb of the internal capsule to the somatosensory cortex (areas 3, 1, 2).
Lesions to the Lateral Spinothalamic Pathway
Spinal cord lesions affecting the Lateral Spinothalamic pathway result in contralateral sensory deficits below the lesion, because the pathway immediately decussates at the second-order neuron level.
Ventral Spinothalamic Pathway
There is also a Ventral Spinothalamic Pathway, that carries crude touch sensation. It is organized very similarly to the Lateral Spinothalamic pathway; however, it is less clinically-emphasized since the Dorsal Column Medial Lemniscus pathway is more important for touch sensation. If the Ventral Spinothalamic pathway is lesioned, touch sensation will only be minimally affected, as long as the dorsal column remains intact.
The basal ganglia are a group of nuclei in the brain stem and are associated with voluntary motor control, procedural learning and emotions.
I’ve decided to go back to the good old days and have one where you can fill in the blanks.
Parkinson’s Disease is a degenerative movement disorder resulting from the death of the dopaminergic neurons in the substantia nigra.
There aren’t any definitive blood tests or imaging for Parkinson’s, so it really comes down to a solid neurological examination.
Generally bradykinesia (slow movement) plus one of the other two cardinal signs
- Rigidity (cogwheel)
- Tremor (pill rolling)
The other movement signs seen in Parkinson’s
- Shuffling gait
- Mask-like expression
- Postural instability: this is tested with the “pull test” – the examiner stands behind the patient and firmly pulls the patient by the shoulders. Someone with normal postural reflexes should only need to take one step back, someone with postural instability will fall or need to take multiple steps backwards.
The Medial Lemniscus-Dorsal Column pathway is an ascending spinal tract, carrying sensory information to the brain. It is typically depicted as a chain of three neurons: first-, second-, and third-order neurons.
This pathway mediates:
- Conscious proprioception (most clinically relevant)
- Sensation of tactile discrimination
- Vibration sense
- Form recognition
First order neurons
The first-order neurons in the pathway are located in the dorsal root ganglia at all spinal levels, giving rise to the fasciculus gracilis tract in the lower extremity and the fasciculus cuneatus tract in the upper extremity. The axons comprising these funiculi ascend ipsilaterally to the medulla, where they synapse with the second-order neurons.
Second order neurons
The second-order neurons are located in the cadual medulla, and their cell bodies form the gracile and cuneate nuclei. Their axons, referred to as internal arcuate fibers, decussate to form the medial lemniscus, which ascends the contralateral brainstem to project to the ventral posterolateral (VPL) nucleus of the thalamus.
Third order neurons
The third-order VPL neurons send axons through the posterior limb of the internal capsule to the somatosensory cortex (areas 3, 1, 2)
Spinal cord lesions affecting the dorsal column (e.g., vitamin B12 neuropathy, tabes dorsalis) result in ipsilateral sensory deficits below the lesion, because the pathway does not decussate until it is at the level of the medulla.
There are 4 main dopamine pathways in the brain:
- Nigro-Striatal: substantial nigra to basal ganglia, involved in movement (what gets affected to cause EPS: tardive dyskinesia, akatisia)
- Meso-Limbic: VTA to nucleus accumbens, “reward” pathway (causes the positive symptoms of schizophrenia)
- Meso-Cortical: VTA to cortex, motivation and emotional response (thought to cause the negative symptoms of schizophrenia)
- Tubulo-Infundibular: hypothalamus to posterior pituitary (hypoprolactinemia in untreated individuals, but D2 blockade with antipsychotics can cause a hyperprolactenemia)
Antipsychotic medication can be divided into 2 classes
- Typical/First Generation
- Atypical/Second Generation
Typicals are characterized by strong D2 antagonism in the mess-limbic and meso-cortical pathways. This can also lead to significant extrapyramidal symptoms (EPS). They also have strong CYP-450 metabolism (which means lots of interactions with other drugs and grapefruits).
- High-potency typicals: only slightly anticholinergic & minimally sedating but have more weight gain and a higher risk of EPS
- Low-potency typicals: more quite sedating and more anticholinergic (bradycardia, GI upset) but have a lower risk of EPS
Atypicals have less risk for EPS, but carry a higher risk for metabolic side-effects and weight gain. While they bind to D2 receptors (like typicals), atypicals have higher affinity for serotonin (5HT) receptors.
Clozapine is a little different from the other atypicals in that is has been shown to have a shorter half-life, which is thought to be why it doesn’t produce as many EPS. However it has the very specific (and serious) risk of agranulocytosis.
When you hit your head on something (or something hits your head) there are two typical patterns of injury. The first is the coupe where the brain injury is directly under the spot that was hit. This usually happens when your head is stationary and something moving hits it (such as someone’s fist).
The second is the contre-coupe, which happens when your head is moving and hits something stationary (such as if you fall and hit your head on the wall or the floor.